Regulation of the mitotic spindle's position is important for cells to divide asymmetrically. Here, we use Caenorhabditis elegans embryos to provide the first analysis of the temporal regulation of forces that asymmetrically position a mitotic spindle. We find that asymmetric pulling forces, regulated by cortical PAR proteins, begin to act as early as prophase and prometaphase, even before the spindle forms and shifts to a posterior position. The spindle does not shift asymmetrically during these early phases due to a tethering force, mediated by astral microtubules that reach the anterior cell cortex. We show that this tether is normally released after spindle assembly and independently of anaphase entry. Monitoring microtubule dynamics by photobleaching segments of microtubules during anaphase revealed that spindle microtubules do not undergo significant poleward flux in C. elegans. Together with the known absence of anaphase A, these data suggest that the major forces contributing to chromosome separation during anaphase originate outside the spindle. We propose that the forces positioning the mitotic spindle asymmetrically are tethered until after the time of spindle assembly and that these same forces are used later to drive chromosome segregation at anaphase.

SummaryWhen a spindle is positioned asymmetrically in a dividing cell, the resulting daughter cells are unequal in size. Asymmetric spindle positioning can be driven by regulated forces that can pull or push a spindle. The physical and molecular mechanisms that can position spindles asymmetrically have been studied in a number of systems, and some themes have begun to emerge from recent research. Recent work in budding yeast has presented a model for how cytoskeletal motors and cortical capture molecules can function in orienting and positioning a spindle. The temporal regulation of microtubule-based pulling forces that move a spindle has been examined in one animal system. Although the spindle positioning force generators have not been identified in most animal systems, the forces have been found to be regulated by both PAR polarity proteins and by G-protein signaling pathways in more than one animal system.

Foraging theory predicts which prey patches predators should target. However, in most habitats, what constitutes a 'patch' and how prey density is calculated are subjective concepts and depend on the spatial scale at which the predator (or scientist) is observing. Moreover, the predator's 'foraging scale' affects prey population dynamics: predators should produce directly density-dependent (DDD) prey mortality at the foraging scale, but inversely density-dependent (IDD) mortality (safety-in-numbers) at smaller scales. We performed the first experimental test of these predictions using behavioral assays with guppies (Poecilia reticulata) feeding on bloodworm 'prey' patches. The guppy's foraging scale had already been estimated in a prior study. Our experimental results confirmed theoretical predictions: predation was IDD when prey were aggregated at a scale smaller than the foraging scale, but not when prey were aggregated at larger scales. These results could be used to predict outcomes of predator-prey interactions in continuous, non-discrete habitats in the field.

The meiotic spindles of animal eggs move to extremely asymmetric positions, close to the cell cortex. A recent paper has identified a motor complex that may move the meiotic spindle toward the cortex in Caenorhabditis elegans eggs.

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